Nasal CPAP in obstructive sleep apnea: mechanisms of action

Sixteen patients with the obstructive sleep apnea syndrome (OSAS) were studied for 1-2 h while receiving continuous positive airway pressure (CPAP) delivered via a nasal mask. Obstructive apneas were obliterated in all. Eight patients had studies of genioglossal muscle activity (GG EMG) and one patient had computed tomograms (CT) of the upper airway while on nasal CPAP. The GG EMG studies showed two patterns: suppression and augmentation of GG EMG while on CPAP. The CT scan showed the airway to be narrowed while the patient was awake off CPAP. It returned to a normal caliber when CPAP was applied, despite sleep. These results are interpreted to suggest three potential mechanisms of action for nasal CPAP in OSAS: 1) reduced upper airway resistance due to prevention of sleep-induced collapse of the airway; 2) reduced upper airway resistance due to dilatation of the airway by nasal CPAP beyond its dimension in the awake state; and 3) possible stimulation of mechanoreceptors leading to an increase in airway tone while CPAP is applied.     

Coronary heart disease and upper airway obstruction

SUMMARY  Coronary heart disease (CHD) is a leading cause of death among middle-aged men. In the same age group the spectrum of upper airway obstruction from habitual snoring to obstructive sleep apnoea syndrome (OSAS) is frequent. In several studies snoring was found to be an important risk factor for ischaemic heart disease. The prevalence of OSAS in patients with CHD, profile of risk factors and ventricular arrhythmias was determined in a prospective manner in 78 patients with stenosis of one or more coronary arteries at coronary arterography. OSAS was found in 27 patients (34.6%). Mean respiratory disturbance index (RDI) was 23.9. RDI increased with higher age. No significant differences in both groups could be found in ventricular arrhythmias, left ventricular ejection fraction and risk factors, except hyperuricaemia and adiposity. OSAS is frequent in patients with CHD and may be an additional risk factor besides the known coronary risk factors. Patients with the combination of CHD and OSAS have to be regarded as a group at particular risk because of several interactions between OSAS and coronary haemodynamics. Furthermore the microstructure of sleep in patients with nocturnal myocardial ischaemia is disturbed.     

Activities of human genioglossus motor units

Upper airway muscles play an important role in regulating airway lumen and in increasing the ability of the pharynx to remain patent in the face of subatmospheric intraluminal pressures produced during inspiration. Due to the considerable technical challenges associated with recording from muscles of the upper airway, much of the experimental work conducted in human subjects has centered on recording respiratory-related activities of the extrinsic tongue protudor muscle, the genioglossus (GG). The GG is one of eight muscles that invest the human tongue (Abd-El-Malek, 1939). All eight muscles are innervated by the hypoglossal nerve (cranial nerve XII) the cell bodies of which are located in the hypoglossal motor nucleus (HMN) of the caudal medulla. Much of the earlier work on the respiratory-related activity of XII motoneurons was based on recordings obtained from single motor axons dissected from the whole XII nerve or from whole muscle GG EMG recordings. Detailed information regarding respiratory-related GG motor unit activities was lacking until as recently as 2006. This paper examines key findings that have emerged from the last decade of work conducted in human subjects. Wherever appropriate, these results are compared with results obtained from in vitro and in vivo studies conducted in non-human mammals. The review is written with the objective of facilitating some discussion and some new thoughts regarding future research directions. The material is framed around four topics: (a) motor unit type, (b) rate coding and recruitment, (c) motor unit activity patterns, and (d) a compartment based view of pharyngeal airway control.     

Tongue mechanical characteristics and genioglossus muscle EMG in obstructive sleep apnoea patients

The increased genioglossus muscle (GGm) activity seen in obstructive sleep apnoea syndrome (OSAS) may lead to increased fatigability or longer recovery time of the tongue. Maximal force, endurance, and recovery times of the tongue, electromyogram (EMG) absolute value, and EMG spectral analysis of the GGm obtained during submaximal contractions were compared in eight individuals without chronic snoring and eight OSAS patients. Endurance time values were not significantly different between the two groups (P = 0.40). Time to recovery of initial maximal force was significantly greater in the OSAS group (P = 0.01). Final EMG median frequency was significantly higher (P = 0.01) and the final low-frequency EMG component smaller in the OSAS patients (P = 0.02). Patients did not have changes in endurance time or fatigability but had longer recovery times and changes in spectral analysis variations. This functional investigation may be helpful in determining the presence of OSAS and the potential contribution of the tongue to pharyngeal obstruction.     

Electromyographic activity at the base and tip of the tongue across sleep–wake states in rats

Obstructive sleep apnea (OSA) patients have elevated tonic and phasic inspiratory activity in the genioglossus and other upper airway muscles during wakefulness; this protects their upper airway from collapse. In this group, sleep-related decrements of upper airway motor tone result in sleep-related upper airway obstructions. We previously reported that in the rat, a species widely used to study the neural mechanisms of both sleep and breathing, lingual electromyographic activity (EMG) is minimal or absent during slow-wave sleep (SWS) and then gradually increases after the onset of rapid eye movement sleep (REMS) due to the appearance of large phasic bursts. Here, we investigated whether sleep–wake patterns and respiratory modulation of lingual EMG depend on the site of EMG recording within the tongue. In nine chronically instrumented rats, we recorded from 17 sites within the tongue and from the diaphragm across sleep–wake states. We quantified lingual EMG in successive 10 s intervals of continuous 2 h recordings (1–3 p.m.). We found that sleep–wake patterns of lingual EMG did not differ between the base and tip of the tongue, and that respiratory modulation was extremely rare regardless of the recording site. We also determined that the often rhythmic lingual bursts during REMS do not occur with respiratory rhythmicity. This pattern differs from that in OSA subjects who, unlike rats, have collapsible upper airway, exhibit prominent respiratory modulation of upper airway motor tone during quiet wakefulness, retain considerable tonic and inspiratory phasic activity during SWS, and show nadirs of activity during REMS.     

Pharyngeal motor control and the pathogenesis of obstructive sleep apnea

The upper airway in patients with obstructive sleep apnea (OSA) is thought to collapse during sleep at least in part, because of a sleep related reduction in upper airway dilator muscle activity. Therefore, a comprehensive understanding of the neural regulation of these muscles is warranted. The dilator muscles can be classified in two broad categories; those that have respiratory related activity and those that fire constantly throughout the respiratory cycle. The motor control of these two groups likely differs with the former receiving input from respiratory neurons and negative pressure reflex circuits. The activity of both muscle groups is reduced shortly after sleep onset, indicating that both receive input from brainstem neurons involved in sleep regulation. In the apnea patient, this may lead to pharyngeal airway collapse. This review briefly describes the currently proposed sleep and respiratory neural pathways and how these circuits interact with the upper airway dilator muscle motorneurones, including recent evidence from animal studies.     

Changes in upper airway resistance during progressive normocapnic hypoxia in patients with obstructive sleep apnoea syndrome

SUMMARY  The responses of the upper airway to progressive normocapnic hypoxia were studied in 6 healthy men and in 6 patients with obstructive sleep apnoea syndrome (OSAS). The upper airway resistance was calculated by the ratio of the laryngeal pressure (measured using a catheter introduced into oesophagus) to the inspiratory flow. Additionally, genioglossal EMG activity (GG-EMG) was measured and analysed. The changes of all variables were analysed individually for each subject. The OSAS patients showed reduced ventilatory response, GG-reactivity and changes in upper airway resistance during progressive hypoxia. It is concluded that impaired reactivity to hypoxic activation (probably due to the process of adaptation of carotid chemoreceptors to nocturnal hypoxia), might reduce the defence abilities of OSAS patients against episodes of obturation in upper airway and obstructive apnoea events.     

Changes in upper airway resistance during progressive normocapnic hypoxia in patients with obstructive sleep apnoea syndrome

The responses of the upper airway to progressive normocapnic hypoxia were studied in 6 healthy men and in 6 patients with obstructive sleep apnoea syndrome (OSAS). The upper airway resistance was calculated by the ratio of the laryngeal pressure (measured using a catheter introduced into oesophagus) to the inspiratory flow. Additionally, genioglossal EMG activity (GG-EMG) was measured and analysed. The changes of all variables were analysed individually for each subject. The OSAS patients showed reduced ventilatory response, GG-reactivity and changes in upper airway resistance during progressive hypoxia. It is concluded that impaired reactivity to hypoxic activation (probably due to the process of adaptation of carotid chemoreceptors to nocturnal hypoxia), might reduce the defence abilities of OSAS patients against episodes of obturation in upper airway and obstructive apnoea events.     

Drive to the human respiratory muscles

The motor control of the respiratory muscles differs in some ways from that of the limb muscles. Effectively, the respiratory muscles are controlled by at least two descending pathways: from the medulla during normal quiet breathing and from the motor cortex during behavioural or voluntary breathing. Neurophysiological studies of single motor unit activity in human subjects during normal and voluntary breathing indicate that the neural drive is not uniform to all muscles. The distribution of neural drive depends on a principle of neuromechanical matching. Those motoneurones that innervate intercostal muscles with greater mechanical advantage are active earlier in the breath and to a greater extent. Inspiratory drive is also distributed differently across different inspiratory muscles, possibly also according to their mechanical effectiveness in developing airway negative pressure. Genioglossus, a muscle of the upper airway, receives various types of neural drive (inspiratory, expiratory and tonic) distributed differentially across the hypoglossal motoneurone pool. The integration of the different inputs results in the overall activity in the muscle to keep the upper airway patent throughout respiration. Integration of respiratory and non-respiratory postural drive can be demonstrated in respiratory muscles, and respiratory drive can even be observed in limb muscles under certain circumstances. Recordings of motor unit activity from the human diaphragm during voluntary respiratory tasks have shown that depending on the task there can be large changes in recruitment threshold and recruitment order of motor units. This suggests that descending drive across the phrenic motoneurone pool is not necessarily consistent. Understanding the integration and distribution of drive to respiratory muscles in automatic breathing and voluntary tasks may have implications for limb motor control.     

肌萎缩侧索硬化患者的腹直肌肌电图检测

目的：探讨腹直肌针极肌电图（EMG）在肌萎缩侧索硬化（ALS）中的诊断价值。方法：对ALS组58例患者进行常规EMG检测,包括上、下肢肌肉、胸锁乳突肌、下胸段脊旁肌及腹直肌,测定自发电位、募集相、运动单位电位（MUP）时限、波幅及多相波,对健康对照组36例健康志愿者进行腹直肌EMG的检测,比较ALS组与对照组腹直肌EMG的差异,以及ALS组中腹直肌EMG与下胸段脊旁肌EMG的差异。结果：健康对照组腹直肌EMG的MUP参数分别为波幅（389±35．7）μV,时限（9．78±1．23）ms,多相波（16．2±5．2）％;ALS组腹直肌EMG的MUP参数分别为波幅（675±135）μV,时限（12．78±1．03）ms,多相波（36．2±7．2）％,ALS组腹直肌EMG各参数与健康对照组比较差异有统计学意义;ALS组腹直肌EMG神经原性改变（43／58,74％）与下胸段脊旁肌EMG（39／58,67％）比较差异无统计学意义。结论：腹直肌EMG各参数均能可靠、稳定地测出,可作为诊断ALS患者胸段下运动神经元病变的辅助手段。     

Does episodic hypoxia affect upper airway dilator muscle function? Implications for the pathophysiology of obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is characterised by repetitive collapse of the upper airway during sleep owing to a sleep-related decrement in upper airway muscle activity with consequent failure of the pharyngeal dilator muscles to oppose the collapsing pressure that is generated by the diaphragm and accessory muscles during inspiration. The causes of upper airway obstruction during sleep are multi-factorial but there is evidence implicating intrinsic upper airway muscle function and impaired central regulation of the upper airway muscles in the pathophysiology of OSA. The condition is associated with episodic hypoxia due to recurrent apnoea. However, despite its obvious importance very little is known about the effects of episodic hypoxia on upper airway muscle function. In this review, we examine the evidence that chronic intermittent hypoxia can affect upper airway muscle structure and function and impair CNS control of the pharyngeal dilator muscles. We review the literature and discuss results from our laboratory showing that episodic hypoxia/asphyxia reduces upper airway muscle endurance and selectively impairs pharyngeal dilator EMG responses to physiological stimulation. Our observations lead us to speculate that episodic hypoxia--a consequence of periodic airway occlusion--is responsible for progression of OSA through impairment of the neural control systems that regulate upper airway patency and through altered respiratory muscle contractile function, leading to the establishment of a vicious cycle of further airway obstruction and hypoxic insult that chronically exacerbates and perpetuates the condition. We conclude that chronic intermittent hypoxia/asphyxia contributes to the pathophysiology of sleep-disordered breathing.     

Shaping appropriate locomotive motor output through interlimb neural pathway within spinal cord in humans

Direct evidence supporting the contribution of upper limb motion on the generation of locomotive motor output in humans is still limited. Here, we aimed to examine the effect of upper limb motion on locomotor-like muscle activities in the lower limb in persons with spinal cord injury (SCI). By imposing passive locomotion-like leg movements, all cervical incomplete (n = 7) and thoracic complete SCI subjects (n = 5) exhibited locomotor-like muscle activity in their paralyzed soleus muscles. Upper limb movements in thoracic complete SCI subjects did not affect the electromyographic (EMG) pattern of the muscle activities. This is quite natural since neural connections in the spinal cord between regions controlling upper and lower limbs were completely lost in these subjects. On the other hand, in cervical incomplete SCI subjects, in whom such neural connections were at least partially preserved, the locomotor-like muscle activity was significantly affected by passively imposed upper limb movements. Specifically, the upper limb movements generally increased the soleus EMG activity during the backward swing phase, which corresponds to the stance phase in normal gait. Although some subjects showed a reduction of the EMG magnitude when arm motion was imposed, this was still consistent with locomotor-like motor output because the reduction of the EMG occurred during the forward swing phase corresponding to the swing phase. The present results indicate that the neural signal induced by the upper limb movements contributes not merely to enhance but also to shape the lower limb locomotive motor output, possibly through interlimb neural pathways. Such neural interaction between upper and lower limb motions could be an underlying neural mechanism of human bipedal locomotion.     

Ischaemic stroke, snoring and obstructive sleep apnoea

SUMMARY  Ischaemic stroke occurs most often during the morning hours before noon. In recent studies the peak time of onset has been between 10.00 and 12.00 hours. Snoring every night or almost every night (habitual snoring) is in relation with ischaemic stroke. Snoring occasionally, on the contrary, is not significantly related with stroke. Habitual snoring is the most typical sign of obstructive sleep apnoea syndrome and it is strongly associated with being overweight. Other possible pathophysiological factors that are in relation with habitual snoring, obstructive sleep apnoea and stroke include arterial hypertension, changes in fibrinolytic activity, adult onset diabetes and smoking. It remains to be seen whether nightly occurring partial upper airway obstruction (habitual snoring) with intrathoracic pressure changes is an independent risk factor of ischaemic stroke. There is recent evidence that everything cannot be explained by other known risk factors.     

平山病的临床与神经电生理学特点分析

目的：分析平山病的临床与神经电生理学特点,以提高对平山病的诊断水平。方法：对21例确诊为平山病的患者进行运动和感觉传导速度、肌电图（EMG）、F波及交感皮肤反应（SSR）等神经电生理学检查。结果：对126条神经进行检测,神经传导速度（NCV）测定总异常率为16．7％（21／126）,主要表现为远端运动潜伏期（DML）延长及复合肌肉动作电位（CMAP）波幅下降,感觉神经传导速度均正常。F波平均最小潜伏期为（28．70±3．10）ms,平均出现率为47．70％,总异常率为76．2％。患者患侧上肢及对侧上肢远端肌（不包括肱桡肌）EMG呈神经原性改变者分别为1000及90．5％,主要异常表现为出现自发电位运动单位电位（MUP）时限延长、波幅增宽、多相波增多及募集相等异常。上肢远端肌EMG异常率为91．5％,明显高于上肢近端肌的8．0％及下肢肌的3．5％。结论：平山病可出现神经电生理上的亚临床改变,神经电生理检查对其有较高的诊断价值。     

Needle electromyography in carpal tunnel syndrome

The role of needle electromyography (EMG) in the routine evaluation of carpal tunnel syndrome (CTS) is not clear. The aim of this study was to determine if needle EMG examination of the thenar muscles could provide useful information in addition to the nerve conduction (NC) studies. Electrophysiologic procedures performed on 84 patients (103 hands) consistent with CTS were reviewed. The median thenar motor NC data were matched with the needle EMG findings in the abductor pollicis brevis (APB) muscle. The severity of the needle EMG findings in the APB muscle correlated well with the severity of the motor NC data. As the thenar compound muscle action potential amplitude decreased and the degree of nerve conduction slowing and block across the wrist increased, there was a corresponding increase in the number of enlarged motor units and decrease in the recruitment pattern in the needle EMG findings. Needle EMG examination confined to the thenar muscles in CTS does not seem to provide any further information when the NC data had already established this diagnosis, and it should not be performed routinely.     

Quantitative magnetic resonance imaging demonstrates alterations of the lingual musculature in obstructive sleep apnea.

Upper airway musculature is important in the pathogenesis of obstructive sleep apnea. Electromyographic studies of patients with obstructive sleep apnea demonstrate increased activity of upper airway dilator muscles. Biopsy studies of these muscles show both adaptation and muscle injury. In this study we utilized quantitative magnetic resonance imaging to characterize changes in the upper airway musculature of patients with obstructive sleep apnea. This technique provides measurements of the T2 relaxation times of upper airway muscles (genioglossus, geniohyoid, sternohyoid/sternothyroid) spatially localized to submillimeter resolution. Our results demonstrate that the mean T2 values of genioglossus (p = 0.04) and geniohyoid (p = 0.06) differ between the apneic and control groups, while the values for the sternohyoid/sternothyroid muscles (p = 0.6) are similar between groups. In both apneics and normals respectively the T2 values for the genioglossus (p = 0.0003, 0.0001) and geniohyoid (p = 0.0054, 0.001) were significantly greater than for the sternohyoid/sternothyroid muscles. The changes observed are compatible with the hypothesis that there is increased edema and possibly increased fat content of the tongue muscles in patients with obstructive sleep apnea.     

Upper airway EMG responses to acute hypoxia and asphyxia are impaired in streptozotocin-induced diabetic rats

Obstructive sleep apnoea (OSA) is a major clinical disorder that is characterised by multiple episodes of upper airway obstruction due to failure of the upper airway dilator muscles to maintain upper airway patency. The incidence of OSA is high in many endocrine disorders including both insulin-dependent and non-insulin-dependent diabetes but the reasons for this are not known. We wished to test the hypothesis that central respiratory motor output to the upper airway muscles is preferentially impaired in a rat model of diabetes mellitus. Sternohyoid (SH) and diaphragm (DIA) EMG activities were recorded in control and streptozotocin (STZ)-induced diabetic rats during normoxia, hypoxia (7.5% O2 in N2) and asphyxia (7.5% O2 and 3% CO2) under pentobarbitone anaesthesia. SH EMG responses to acute hypoxia and asphyxia were significantly impaired in STZ-induced diabetic rats compared to control animals (+47.1 +/- 5.7 vs. +11.7 +/- 1.9% during hypoxia in control and diabetic animals respectively and +56.5 +/- 7.9 vs. +15.7 +/- 5.0% during asphyxia). However, DIA EMG responses to hypoxia and asphyxia were not different for the two groups. We propose that the higher prevalence of OSA in diabetic patients is related to preferential impairment of cranial motor output to the dilator muscles of the upper airway in response to physiological stimuli.     

Disintegration of the motor unit in post-polio syndrome. Part II. Electrophysiological findings in patients with post-polio syndrome

The aim of the study is to investigate the motor unit abnormalities in late postpolio muscular atrophy (PPMA) as compared to those found in patients who had polio 20-30 years prior to examination without any new clinical signs. The quantitative concentric needle EMG and a single fiber EMG techniques were employed. Spontaneous activity, the parameters of individual motor units potentials (MUP), number of complex potentials and their stability, jitter and blocking as well as fiber density (FD) have been evaluated. In PPMA patients (5 subjects) we found in newly weakened muscles: spontaneous activity, high percentage of complex potentials, increased jitter, increased FD. The EMG findings in muscles previously affected but without any signs of progression have been similar. In the patients with stable nonprogressing postpolio muscle atrophy (12) all MUP-s parameters indicated changes similar to PPMA but less marked in initially affected muscle with complete or incomplete recovery as well as sometimes in initially clinically unaffected muscles. These findings suggest that the signs of ongoing reinnervation processes persist many years after polio and that PPMA occurring later in life represents disintegration of the previously reinnervated motor units. It is still unclear whether this disintegration depends on decompensation by different factors of fully reinnervated motor units or whether most of the motor units after polio never regained a stable reinnervation.     

Effects of nasal pathologies on obstructive sleep apnea

Increased airway resistance can induce snoring and sleep apnea, and nasal obstruction is a common problem in snoring and obstructive sleep apnea (OSA) patients. Many snoring and OSA patients breathe via the mouth during sleep. Mouth breathing may contribute to increased collapsibility of the upper airways due to decreased contractile efficiency of the upper airway muscles as a result of mouth opening. Increased nasal airway resistance produces turbulent flow in the nasal cavity, induces oral breathing, promotes oscillation of the pharyngeal airway and can cause snoring.     

Evidence for bilateral innervation of certain homologous motoneurone pools in man.

1. Surface EMG recordings were made from left and right homologous muscle pairs in healthy adults. During each recording session subjects were requested to maintain a weak isometric contraction of both the left and right muscle. 2. Cross-correlation analysis of the two multiunit EMG recordings from each pair of muscles was performed. Central peaks of short duration (mean durations, 11.3-13.0 ms) were seen in correlograms constructed from multiunit EMG recordings obtained from left and right diaphragm, rectus abdominis and masseter muscles. No central peaks were seen in correlograms constructed from the multiunit EMG recordings from left and right upper limb muscles. 3. To investigate descending pathways to the homologous muscle pairs, the dominant motor cortex was stimulated using a focal magnetic brain stimulator whilst recording from homologous muscle pairs. 4. Following magnetic stimulation of the dominant motor cortex, a response was recorded from both right and left diaphragm, rectus abdominis and masseter muscles. In contrast, when recording from homologous upper limb muscles, a response was only seen contralateral to the side of stimulation. 5. The finding of short duration central peaks in the cross-correlograms constructed from multiunit recordings from left and right diaphragm, rectus abdominis and masseter, suggests that muscles such as these, that are normally co-activated, share a common drive. The mechanism is discussed and it is argued that the time course of the central correlogram peaks is consistent with the hypothesis that they could be produced by a common drive that arises from activity in last-order branched presynaptic fibres although presynaptic synchronization of last-order inputs is also likely to be involved. 6. The results of the magnetic stimulation experiments suggest that this common drive may involve the corticospinal tract. 7. We saw no evidence for a common drive to left and right homologous muscle pairs that may be voluntarily co-activated but often act independently.